The gut is an important reservoir for drug-resistant bacteria responsible for life-threatening hospital-acquired infections. A new study (in mice) suggests that two of the most common antibiotic-resistant bacterial species circulating in hospitals occupy effectively share the same location in the gut, and that they can be eliminated by faecal transplantation of a healthy gut microbiome.

This paper investigates the interactions between vancomycin-resistant Enterococcus faecium (VRE) and multi-drug resistant Klebsiella pneumoniae in the intestine. Together, the two pathogens are responsible for about 10% of serious hospital-acquired infections. Both can colonize the gut and spread from there, to the same or other patients, to cause localized or systemic infections.

It is known that transplantation of faeces from healthy mice can eliminate VRE from the intestine of densely colonized mice and, in humans, faecal transplantation from healthy donors can cure patients with certain pathogenic intestinal infections. To determine whether faecal transplantation can clear K. pneumoniae and concurrent VRE and K. pneumoniae infections, the researchers colonized mice with VRE and K. pneumoniae concurrently and then treated them with faecal microbiota transplants or a sterile control solution on three consecutive days. Following FMT treatment, K. pneumoniae in faecal pellets decreased within one day and became undetectable within 7 days. VRE was cleared in 60% of the mice and reduced by a thousand-fold in the remaining 40%.

Would this method work in humans? There’s no reason to think not, but there’s only one way to find out…

Distinct but Spatially Overlapping Intestinal Niches for Vancomycin-Resistant Enterococcus faecium and Carbapenem-Resistant Klebsiella pneumoniae. (2015) PLoS Pathogens 11(9): e1005132. doi: 10.1371/journal.ppat.1005132
Antibiotic resistance among enterococci and γ-proteobacteria is an increasing problem in healthcare settings. Dense colonization of the gut by antibiotic-resistant bacteria facilitates their spread between patients and also leads to bloodstream and other systemic infections. Antibiotic-mediated destruction of the intestinal microbiota and consequent loss of colonization resistance are critical factors leading to persistence and spread of antibiotic-resistant bacteria. The mechanisms underlying microbiota-mediated colonization resistance remain incompletely defined and are likely distinct for different antibiotic-resistant bacterial species. It is unclear whether enterococci or γ-proteobacteria, upon expanding to high density in the gut, confer colonization resistance against competing bacterial species. Herein, we demonstrate that dense intestinal colonization with vancomycin-resistant Enterococcus faecium (VRE) does not reduce in vivo growth of carbapenem-resistant Klebsiella pneumoniae. Reciprocally, K. pneumoniae does not impair intestinal colonization by VRE. In contrast, transplantation of a diverse fecal microbiota eliminates both VRE and K. pneumoniae from the gut. Fluorescence in situ hybridization demonstrates that VRE and K. pneumoniae localize to the same regions in the colon but differ with respect to stimulation and invasion of the colonic mucus layer. While VRE and K. pneumoniae occupy the same three-dimensional space within the gut lumen, their independent growth and persistence in the gut suggests that they reside in distinct niches that satisfy their specific in vivo metabolic needs.